Short- and long-term survival after isolated coronary artery bypass grafting, the impact of gender and age.

Objectives. Assess the short- and long-term survival for patients who underwent isolated coronary artery bypass grafting (CABG) and evaluate the impact of gender and age. Furthermore to assess the long-term survival in the CABG group compared to the general population. Design. This study included 4044 consecutive patients who underwent isolated CABG at Oslo University Hospital, Ullevål, in Oslo, Norway in the time period from 01 January 2003 to 31 December 2015. Patient data was collected retrospectively from the quality register at the department. Information on survival status was obtained from the Norwegian National Registry. Life expectancy data for the general population was gained from Statistics Norway. Results. Female patients were significantly older than male patients at the time of surgery (mean age 67.0 and 63.9 years, respectively, p < .001), and had significantly lower 30-day survival (mortality was 1.4% and 0.6%, respectively, p = .017). Male gender was independently associated with lower long-term survival (p = .0037) in a multivariate analysis. Male patients aged less than 60 years also showed significantly lower long-term survival (SMR = 1.84, 95% CI = 1.49-2.25) compared to the age-matched general population. Among patients older than 60 years, survival was similar to survival in the age-matched general population. Conclusions. Survival was excellent for patients undergoing surgery. Despite increased age and operative mortality, female patients had better adjusted long-time survival than male patients. There was lower long-term survival among male patients aged less than 60 compared to the general population. Our findings may help clinicians in selecting appropriate patients for surgery.

Reduced visfatin levels in aortic stenosis increase after aortic valve replacement and may contribute to reverse left ventricular remodelling.

AIM: Visfatin may play a part in reverse left ventricular remodelling. Using a mouse model of reversible left ventricle pressure overload, we examined if visfatin was altered in the myocardium. Furthermore, we addressed this issue in patients with aortic stenosis (AS) and examined whether visfatin levels are related to reverse remodelling following aortic valve replacement (AVR). METHODS: Myocardial visfatin was analysed after aortic banding (AB) and debanding (DB) in mice and compared to sham operated animals. Myocardial visfatin was measured in biopsies from patients undergoing AVR and compared to controls. Serum visfatin was measured before and after AVR in patients with AS and correlated with echocardiographic measurments of cardiac morphology and function. RESULTS: Four weeks after AB, myocardial visfatin protein was reduced by 50% compared to sham. Three days after DB, myocardial protein levels increased significantly. Myocardial visfatin and serum visfatin levels were reduced by 23% and 64%, respectively, in patients with AS compared to controls. Twelve months after AVR, serum visfatin levels increased compared to preoperative values and correlated negatively with degree of left ventricular hypertrophy. CONCLUSION: Myocardial visfatin and serum visfatin levels are reduced by cardiac pressure overload. Visfatin levels increase after correction of pressure overload and may play a part in postoperative reverse remodelling.

A mouse model of reverse cardiac remodelling following banding-debanding of the ascending aorta.

AIM: Myocardial remodelling during pressure overload might contribute to development of heart failure. Reverse remodelling normally occurs following aortic valve replacement for aortic stenosis; however, the details and regulatory mechanisms of reverse remodelling remain unknown. Thus, an experimental model of reverse remodelling would allow for studies of this process. Although models of aortic banding are widely used, only few reports of debanding models exist. The aim of this study was to establish a banding-debanding model in the mouse with repetitive careful haemodynamic evaluation by high-resolution echocardiography. METHODS: C57Bl/6 mice were subjected to ascending aortic banding and subsequent debanding. Cardiac geometry and function were evaluated by echocardiography, and left ventricular myocardium was analysed by histology and quantitative real-time polymerase chain reaction. RESULTS: The degree of aortic banding was controlled by non-invasive estimation of the gradient, and we found a close correlation between left ventricular mass estimated by echocardiography and weight at the time of killing. Aortic banding led to left ventricular hypertrophy, fibrosis and expression of foetal genes, indicating myocardial remodelling. Echocardiography revealed concentric left ventricular remodelling and myocardial dysfunction. Following debanding, performed via a different incision, there was rapid regression of left ventricular weight and normalization of both cardiac geometry and function by 14 days. CONCLUSIONS: We have established a reproducible and carefully characterized mouse model of reverse remodelling by banding and debanding of the ascending aorta. Such a model might contribute to increased understanding of the reversibility of cardiac pathology, which in turn might give rise to new strategies in heart failure treatment.